At puberty the cervix is exposed to estrogen and progesterone which are thought to stimulate a shift of endocervical columnar cells onto the ectocervix (cervical ectopy). The vaginal ph which is lowered at puberty promotes squamous metaplasia whereby ectocervical columnar cells are replaced by squamous epithelium. With time the number of columnar cells on the ectocervix decreases, thus, decreasing the area of ectopy. Sexual activity may also increase metaplasia. In the first aim, using cervical photographs, we will evaluate the change in the amount of ectopy by years since the first menstrual period in sexually active adolescents, adjusting for sexual activity and sexually transmitted diseases. Progesterone induces microglandular hyperplasia (growth of columnar cells), protrusion of endocervical columnar cells and stromal edema, and estradiol induces hyperemia of the uterus. While oral contraceptives (OCs) may produce cervical ectopy by any of these mechanisms the contributions of each of these hormones individually is unclear. The second aim is to compare in adolescents the effects of OCs (estrogen and progestin) with Depo Provera (progestin) on cervical ectopy using cervical photographs. Adolesecents have a high prevalence of ectopy. Both OC users and Depo users will be compared with never users of hormonal contraceptives. Cervical ectopy is associated with an increased risk of chlamydial infection. The third aim is to determine whether a greater area of columnar cells on the ectocervix is associated with an increased rate of chlamydial infection, perhaps by increasing the opportunity for infection or propagation.